| Project/Area Number |
15K19469
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Kidney internal medicine
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| Research Institution | Tokai University |
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Principal Investigator |
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 内分泌学 / 副甲状腺機能亢進症 / シナカルセト塩酸塩 / 二次性副甲状腺機能亢進症 / 細胞周期 |
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| Outline of Final Research Achievements |
Cinacalcet hydrochloride is an activator of calcium-sensing receptor and used for therapies of hyperparathyroidism. In the previous study, we reported that intermittent administrations of cinacalcet for long periods promoted apoptosis in hyperpalsia of parathyroid glands. Now, we examined the mechanism of the induction of apoptosis by comparing parathyroid specimens between cinacalcet-administrated and non-administrated patients. Immunohistochemistry showed a decrease of p27Kip1 expression and an increase of cells expressing c-myc in cinacalcet-administrated parathyroids, which indicated an induction of re-entry into cell-cycle from G0 static phase. A part of c-myc expressing cells co-expressed an apoptosis marker, caspase-3. These results indicated that cinacalcet induced some of static parathyroid cells to re-enter into cell cycle, but a part of them could not go through checkpoints in the way of cell cycle and followed the apoptosis route, which led the regression of glands.
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